The effects of nutrition, oxidation, and other environmental factors (light intensity or darkness) on incidence and progress of posterior subcapsular opacities (PSO) associated with retinal degeneration are being studied in pink-eyed Royal College of Surgeons (RCS) rats, in which rod photoreceptor outer segment debris accumulates secondary to a phagocytic defect in retinal pigmented epithelium. Evidence was obtained that oxidative changes in polyunsaturated fatty acids in debris led to water-soluble toxic aldehydes, detectable in the vitreous and toxic to lens cells and membranes. Dystrophic rats fed a natural ingredient diet (NIH-07) are highly susceptible to retinal light damage, beginning at 1-4 footcandles (fc) intensity: 27% of the rats develop mature cataracts by 7-12 months. Increased light intensity (cyclic or constant) increased the percentage of rats with mature cataracts, while dark-rearing from birth prevented PSO and mature cataracts. A purified diet (AIN-76A), fortified with 0.4% beta-carotene + 0.01% BHT, also prevented PSO and mature cataracts. Rhodopsin bleaching appears to be essential for retinal light damage and PSO. A 100% incidence of bilateral mature cataracts occurred in dystrophic rats given 48 hours of 700-fc constant light between postnatal days 22 and 28, when rhodopsin is increased 70% in debris. A similar incidence of bilateral cataracts occurred in congenic control RCS rats given 18 days of dark adaptation to increase rhodopsin by 50%, followed by the same constant light exposure. In vitro, free retinaldehyde can act as a photosensitizer to generate singlet oxygen, an extremely energetic oxidant. Present results suggest a similar effect in vivo, with damage to both lipids and proteins. Current studies are directed toward exploring how many days retinal degeneration can be delayed by different antioxidant-containing diets. Antioxidants may slow or prevent cataracts in some human retinal diseases.